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1,263 results on '"Jackson, Edwin K."'

202. Critical Role for the Adenosine Pathway in Controlling Simian Immunodeficiency Virus-Related Immune Activation and Inflammation in Gut Mucosal Tissues

Author

He, Tianyu, primary, Brocca-Cofano, Egidio, additional, Gillespie, Delbert G., additional, Xu, Cuiling, additional, Stock, Jennifer L., additional, Ma, Dongzhu, additional, Policicchio, Benjamin B., additional, Raehtz, Kevin D., additional, Rinaldo, Charles R., additional, Apetrei, Cristian, additional, Jackson, Edwin K., additional, Macatangay, Bernard J. C., additional, and Pandrea, Ivona, additional

Published
2015
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204. Estradiol Stimulates Capillary Formation by Human Endothelial Progenitor Cells: Role of ER-α/β, Heme Oxygenase-1 and Tyrosine Kinase

Author

Baruscotti, Isabella, Barchiesi, Federica, Jackson, Edwin K, Imthurn, Bruno, Stiller, Ruth, Kim, Jai-Hyun, Schaufelberger, Sara, Rosselli, Marinella, Hughes, Christopher CW, and Dubey, Raghvendra K.

Subjects
Analysis of Variance, Mitogen-Activated Protein Kinase 3, Estradiol, Stem Cells, Blotting, Western, Estrogen Receptor alpha, Endothelial Cells, Neovascularization, Physiologic, Enzyme-Linked Immunosorbent Assay, Protein-Tyrosine Kinases, Flow Cytometry, Article, Capillaries, Receptors, Vascular Endothelial Growth Factor, Estrogen Receptor beta, Humans, Phosphorylation, Proto-Oncogene Proteins c-akt, hormones, hormone substitutes, and hormone antagonists, Heme Oxygenase-1, Signal Transduction
Abstract

Endothelial progenitor cells (EPCs) repair damaged endothelium and promote capillary formation, processes involving receptor tyrosine kinases (RTKs) and heme oxygenase 1 (HO-1). Because estradiol augments vascular repair, we hypothesize that estradiol increases EPC proliferation and capillary formation via RTK activation and induction of HO-1. Physiological concentrations of estradiol (10 nmol/L) increased EPC-induced capillary sprout and lumen formation in matrigel/fibrin/collagen systems. Propyl-pyrazole-triol (PPT; 100 nmol/L; estrogen receptor [ER]-alpha agonist), but not diarylpropionitrile (ER-beta agonist), mimicked the stimulatory effects of estradiol on capillary formation, and methyl-piperidino-pyrazole (ER-alpha antagonist) abolished the effects of estradiol and PPT. Three different RTK activators (vascular endothelial growth factor, hepatocyte growth factor, and stromal derived growth factor 1) mimicked the capillary-stimulating effects of estradiol and PPT. SU5416 (RTK inhibitor) blocked the stimulatory effects of estradiol and PPT on capillary formation. Estradiol increased HO-1 expression by 2- to 3-fold, an effect blocked by SU5416, and PPT mimicked the effects of estradiol on HO-1. The ability of estradiol to enhance capillary formation, increase expression of HO-1, and augment phosphorylation of extracellular signal-regulated kinase 1/2, Akt, and vascular endothelial growth factor receptor 2 was mimicked by its cell-impermeable analog BSA estradiol. Actinomycin (transcription inhibitor) did not alter the effects of estradiol on RTK activity or vascular endothelial growth factor secretion. We conclude that estradiol via ER-alpha promotes EPC-mediated capillary formation by a mechanism that involves nongenomic activation of RTKs and HO-1 activation. Estradiol in particular and ER-alpha agonists in general may promote healing of injured vascular beds by promoting EPC activity leading to more rapid endothelial recovery and capillary formation after injury.

Published
2010

205. Structure Guided Chemical Modifications of Propylthiouracil Reveal Novel Small Molecule Inhibitors of Cytochrome b5 Reductase 3 That Increase Nitric Oxide Bioavailability

Author

Rahaman, Md. Mizanur, primary, Reinders, Fabio G., additional, Koes, David, additional, Nguyen, Anh T., additional, Mutchler, Stephanie M., additional, Sparacino-Watkins, Courtney, additional, Alvarez, Roger A., additional, Miller, Megan P., additional, Cheng, Dongmei, additional, Chen, Bill B., additional, Jackson, Edwin K., additional, Camacho, Carlos J., additional, and Straub, Adam C., additional

Published
2015
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207. Adenosin-vermittelte Immunsuppression in Patienten mit Plattenepithelkarinomen des Kopf-Hals-Bereichs

Author

Mandapathil, Magis, Szczepanski, Miroslaw, Johnson, Jonas T, Jackson, Edwin K, Gorelik, Elisier, Lang, Stefan, and Whiteside, Theresa L

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Trotz Verbesserung in verschiedenen Behandlungsoptionen des HNSCC, bleibt die Langzeitprognose schlecht. Ursache hierfür ist u.a. die Hemmung des Immunsystems durch den Tumor und regulatorischen T Zellen (Treg). Die Mechanismen zur Immunsuppression, die Treg und Tumore anwenden sind jedoch unklar.[for full text, please go to the a.m. URL], 81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie

Published
2010

209. Immunological mechanisms of the antitumor effects of supplemental oxygenation

Author

Hatfield, Stephen M., primary, Kjaergaard, Jorgen, additional, Lukashev, Dmitriy, additional, Schreiber, Taylor H., additional, Belikoff, Bryan, additional, Abbott, Robert, additional, Sethumadhavan, Shalini, additional, Philbrook, Phaethon, additional, Ko, Kami, additional, Cannici, Ryan, additional, Thayer, Molly, additional, Rodig, Scott, additional, Kutok, Jeffrey L., additional, Jackson, Edwin K., additional, Karger, Barry, additional, Podack, Eckhard R., additional, Ohta, Akio, additional, and Sitkovsky, Michail V., additional

Published
2015
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211. Prevention of Skin Carcinogenesis by the β-Blocker Carvedilol

Author

Chang, Andy, primary, Yeung, Steven, additional, Thakkar, Arvind, additional, Huang, Kevin M., additional, Liu, Mandy M., additional, Kanassatega, Rhye-Samuel, additional, Parsa, Cyrus, additional, Orlando, Robert, additional, Jackson, Edwin K., additional, Andresen, Bradley T., additional, and Huang, Ying, additional

Published
2015
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215. Multidrug Resistance Protein 4 Mediates 3’,5,-cAMP Efflux From Rat Preglomerular Vascular Smooth Muscle Cells

Author

Cheng, Dongmei, Ren, Jin, and Jackson, Edwin K.

Subjects
Cyclic AMP, Isoproterenol, Animals, RNA Interference, Multidrug Resistance-Associated Proteins, Kidney, Article, Muscle, Smooth, Vascular, Rats
Abstract

1. Previous studies have shown that stimulation of adenylyl cyclase in preglomerular vascular smooth muscle cells (PGVSMC) increases extracellular cAMP; however, the mechanism by which PGVSMC transport intracellular cAMP into the extracellular milieu is unknown. 2. We hypothesize that multidrug resistance protein (MRP) 4 is the primary transporter mediating efflux of intracellular cAMP from PGVSMC. 3. Both reverse transcription-polymerase chain reaction and real-time polymerase chain reaction detected MRP4 mRNA in PGVSMC in culture. Moreover, western blotting using an antibody specific for MRP4 gave rise to a 150 kDa signal, consistent with the presence of MRP4 protein in PGVSMC. 4. Specifically designed short interference (si) RNA reduced MRP4 mRNA expression by 71% (P = 0.0075) and MRP4 protein by 80% (P = 0.0004). 5. Isoproterenol (1 micromol/L) increased intracellular cAMP, which resulted in efflux of cAMP into the medium. The siRNA knockdown of MRP4 significantly reduced basal extracellular cAMP and nearly abolished isoproterenol-induced increases in extracellular cAMP (P = 0.0143, interaction between isoproterenol and MRP4 siRNA in two-factor analysis of variance). In isoproterenol-treated cells, MRP4 siRNA decreased the ratio of extracellular cAMP to intracellular cAMP by 72% (P = 0.0019). 6. We conclude that MRP4 is the dominant cAMP transporter in PGVSMC.

Published
2009

216. RACK1 regulates angiotensin II-induced contractions of SHR preglomerular vascular smooth muscle cells.

Author

Xiao Zhu and Jackson, Edwin K.

Subjects
*VASCULAR smooth muscle contraction, *ANGIOTENSIN II, *G proteins
Abstract

The preglomerular microcirculation of spontaneously hypertensive rats (SHR) is hypersensitive to angiotensin (ANG) II, and studies have shown that this is likely due to enhanced coincident signaling between G protein subunits αq (Gαq; released by ANG II) and βγ (Gβγ released by Gi-coupled receptors) to active phospholipase C (PLC). Here we investigated the molecular basis for the enhanced coincident signaling between Gβγ and Gαq in SHR preglomerular vascular smooth muscle cells (PGVSMCs). Because receptor for activated C kinase 1 (RACK1; a scaffolding protein) organizes interactions between Gβγ, Gαq, and PLC, we included RACK1 in this investigation. Cell fractionation studies demonstrated increased levels of membrane (but not cytosolic) Gγ, Gαq, PLCγ3, and RACK1 in SHR PGVSMCs compared with Wistar-Kyoto rat PGVSMCs. In SHR PGVSMCs, coimmunoprecipitation demonstrated RACK1 binding to Gγ and PLCγ3, but only at cell membranes. Pertussis toxin (which blocks Gβγ) and U73122 (which blocks PLC) reduced membrane RACK1; however, RACK1 knockdown (shRNA) did not affect membrane levels of Gγ, Gαq, or PLCγ3. In a novel gel contraction assay, RACK1 knockdown in SHR PGVSMCs attenuated contractions to ANG II and abrogated the ability of neuropeptide Y (which signals via Gβγ) to enhance ANG II-induced contractions. We conclude that in SHR PGVSMCs the enlarged pool of Gβγ and PLCγ3 recruits RACK1 to membranes and RACK1 then organizes signaling. Consequently, knockdown of RACK1 prevents coincident signaling between ANG II and the Gi pathway. This is the first study to implicate RACK1 in vascular smooth muscle cell contraction and suggests that RACK1 inhibitors could be effective cardiovascular drugs. [ABSTRACT FROM AUTHOR]

Published
2017
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222. Hemorrhagic Shock Shifts the Serum Cytokine Profile from Pro- to Anti-Inflammatory after Experimental Traumatic Brain Injury in Mice

Author

Shein, Steven L., primary, Shellington, David K., additional, Exo, Jennifer L., additional, Jackson, Travis C., additional, Wisniewski, Stephen R., additional, Jackson, Edwin K., additional, Vagni, Vincent A., additional, Bayır, Hülya, additional, Clark, Robert S.B., additional, Dixon, C. Edward, additional, Janesko-Feldman, Keri L., additional, and Kochanek, Patrick M., additional

Published
2014
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227. Clinical implications of prostaglandin and thromboxane A2 formation

Author

Oates, John A., FitzGerald, Garret A., Branch, Robert A., Jackson, Edwin K., Knapp, Howard R., and Roberts, L. Jackson, II

Subjects
Blood pressure -- Measurement, Thromboxanes -- Physiological aspects, Nonsteroidal anti-inflammatory drugs -- Physiological aspects, Prostaglandins -- Physiological aspects, Hypertension -- Drug therapy
Published
1988

228. Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Author

UNIFORMED SERVICES UNIV OF THE HEALTH SCIENCES BETHESDA MD, Kochanek, Patrick M, Dixon, C E, Shellington, David K, Shin, Samuel S, Bayir, Hulya, Jackson, Edwin K, Kagan, Valerian E, Yan, Hong Q, Swauger, Peter V, Parks, Steven A, UNIFORMED SERVICES UNIV OF THE HEALTH SCIENCES BETHESDA MD, Kochanek, Patrick M, Dixon, C E, Shellington, David K, Shin, Samuel S, Bayir, Hulya, Jackson, Edwin K, Kagan, Valerian E, Yan, Hong Q, Swauger, Peter V, and Parks, Steven A

Abstract

Explosive Blast-induced traumatic brain injury (TBI) is the signature insult in modern combat casualty care and has been linked to posttraumatic stress disorder, memory loss, and chronic traumatic encephalopathy. We reported on blast induced mild TBI (mTBI) characterized by fiber-tract degeneration and axonal injury revealed by cupric silver staining in adult male rats after head only exposure to 35 PSI in a helium-driven shock tube with head restraint. We now explore pathways of secondary injury and repair using biochemical/molecular strategies. Injury produced approx. 25% mortality from apnea. Shams received identical anesthesia exposure. Rats were sacrificed at 2h or 24h and brain sampled in hippocampus and pre-frontal cortex. Hippocampal samples were used to assess gene array (RatRef-12 Expression BeadChip) and oxidative stress (ascorbate, glutathione [GSH], low molecular weight thiols [LMWT], protein thiols, and 4-hydroxynonenal [HNE]). Cortical samples were used to assess neuroinflammation (cytokines, chemokines, and growth factors; Luminex) and purines (ATP, ADP, adenosine, inosine, 2 -AMP, and 5 -AMP). Gene array revealed marked increases in astrocyte and neuroinflammatory markers at 24h (GFAP, Vimentin, complement component 1) with expression patterns bioinformatically consistent with those seen in Alzheimer s disease and long-term potentiation. Ascorbate, LMWT, and protein thiols were reduced at 2 and 24h; by 24h HNE was increased. At 2h, multiple cytokines and chemokines (IL-1alpha, IL-6, IL-10, MIP-1alpha), were increased; by 24h only MIP-1alpha remained elevated. ATP was not depleted and adenosine correlated with 2 - not 5 -cAMP. Our data reveal; (1) gene array alterations similar to disorders of memory processing and a marked astrocyte response, (2) oxidative stress, 2) neuroinflammation with a sustained chemokine response, and (3) adenosine production despite lack of energy failure possibly resulting from metabolism of 2 -3 -cAMP., Published in the Journal of Neurotrauma, Preprint, p1-64, 17 March 2013. The original document contains color images.

Published
2013

229. Pharmacological Inhibition of Pleckstrin Homology Domain Leucine-Rich Repeat Protein Phosphatase Is Neuroprotective: Differential Effects on Astrocytes

Author

Jackson, Travis C., primary, Verrier, Jonathan D., additional, Drabek, Tomas, additional, Janesko-Feldman, Keri, additional, Gillespie, Delbert G., additional, Uray, Thomas, additional, Dezfulian, Cameron, additional, Clark, Robert S., additional, Bayir, Hülya, additional, Jackson, Edwin K., additional, and Kochanek, Patrick M., additional

Published
2013
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231. The β-blocker Nebivolol Is a GRK/β-arrestin Biased Agonist

Author

Erickson, Catherine E., primary, Gul, Rukhsana, additional, Blessing, Christopher P., additional, Nguyen, Jenny, additional, Liu, Tammy, additional, Pulakat, Lakshmi, additional, Bastepe, Murat, additional, Jackson, Edwin K., additional, and Andresen, Bradley T., additional

Published
2013
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235. Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Author

Kochanek, Patrick M., primary, Dixon, C. Edward, additional, Shellington, David K., additional, Shin, Samuel S., additional, Bayır, Hülya, additional, Jackson, Edwin K., additional, Kagan, Valerian E., additional, Yan, Hong Q., additional, Swauger, Peter V., additional, Parks, Steven A., additional, Ritzel, David V., additional, Bauman, Richard, additional, Clark, Robert S.B., additional, Garman, Robert H., additional, Bandak, Faris, additional, Ling, Geoffrey, additional, and Jenkins, Larry W., additional

Published
2013
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242. Purines: forgotten mediators in traumatic brain injury.

Author

Jackson, Edwin K., Boison, Detlev, Schwarzschild, Michael A., and Kochanek, Patrick M.

Subjects
*PURINES, *BRAIN injuries, *NEUROCHEMISTRY, *NEURODEGENERATION, *SPASMS, *EPILEPSY, *CENTRAL nervous system injuries, *THERAPEUTICS
Abstract

Recently, the topic of traumatic brain injury has gained attention in both the scientific community and lay press. Similarly, there have been exciting developments on multiple fronts in the area of neurochemistry specifically related to purine biology that are relevant to both neuroprotection and neurodegeneration. At the 2105 meeting of the National Neurotrauma Society, a session sponsored by the International Society for Neurochemistry featured three experts in the field of purine biology who discussed new developments that are germane to both the pathomechanisms of secondary injury and development of therapies for traumatic brain injury. This included presentations by Drs. Edwin Jackson on the novel 2′,3′-cAMP pathway in neuroprotection, Detlev Boison on adenosine in post-traumatic seizures and epilepsy, and Michael Schwarzschild on the potential of urate to treat central nervous system injury. This mini review summarizes the important findings in these three areas and outlines future directions for the development of new purine-related therapies for traumatic brain injury and other forms of central nervous system injury. [ABSTRACT FROM AUTHOR]

Published
2016
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243. In Vivo Hypoxic Preconditioning Protects From Warm Liver Ischemia-Reperfusion Injury Through the Adenosine A2B Receptor

Author

Choukèr, Alexander, primary, Ohta, Akio, additional, Martignoni, André, additional, Lukashev, Dmitriy, additional, Zacharia, Lefteris C., additional, Jackson, Edwin K., additional, Schnermann, Jürgen, additional, Ward, Jerrold M., additional, Kaufmann, Ines, additional, Klaunberg, Brenda, additional, Sitkovsky, Michail V., additional, and Thiel, Manfred, additional

Published
2012
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248. CD26 expression and adenosine deaminase activity in regulatory T cells (Treg) and CD4+T effector cells in patients with head and neck squamous cell carcinoma

Author

Mandapathil, Magis, primary, Szczepanski, Miroslaw, additional, Harasymczuk, Malgorzata, additional, Ren, Jin, additional, Cheng, Dongmei, additional, Jackson, Edwin K., additional, Gorelik, Elieser, additional, Johnson, Jonas, additional, Lang, Stephan, additional, and Whiteside, Theresa L, additional

Published
2012
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250. Microglial depletion using intrahippocampal injection of liposome-encapsulated clodronate in prolonged hypothermic cardiac arrest in rats

Author

Drabek, Tomas, primary, Janata, Andreas, additional, Jackson, Edwin K., additional, End, Brad, additional, Stezoski, Jason, additional, Vagni, Vincent A., additional, Janesko-Feldman, Keri, additional, Wilson, Caleb D., additional, van Rooijen, Nico, additional, Tisherman, Samuel A., additional, and Kochanek, Patrick M., additional

Published
2012
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